Amebiasis has a worldwide distribution.

It is the third most common cause of death from

parasitic infection in the world, although serious disease in the United States is uncommon.
Cutaneous manifestations of the infection are rare. Although skin lesions can occur in any
location, anogenital ulcers are the most commonly reported cutaneous manifestation in children,
generally a result of direct inoculation from infected stool. Cutaneous amebiasis often portends a
poor prognosis. Without a high index of suspicion, and therefore prompt diagnosis and treatment,
it can result in serious morbidity and even death.

Cutaneous amebiasis is a rarely reported clinical manifestation of E histolytica infection.

In a review of 5,097 patients with invasive amebiasis admitted to a South African hospital, only
two cases with cutaneous involvement were noted. The perineovulvar area is the most common
site of the cutaneous lesions, probably because of prolonged and repeated skin contact with
discharges containing virulent trophozoites of E histolytica.

The E. histolytica life cycle is composed of two main stages: the disease-producing,
invasive trophozoite or the infective cyst. Trophozoites can survive in human stool, and invade
the colonic wall by either binding to epithelial cells on the mucosal surface, whereby they release
cytotoxins, causing cell lysis, or by phagocytosis of red blood cells and polymorphonuclear
neutrophils . Trophozoites can subsequently invade blood vessels and undergo hematogenous
dissemination, sometimes to the liver and lungs. Alternatively, trophozoites can develop into
infective cysts by binary fission. Cysts are then passed in the stool and contaminate food and
water. Following human ingestion, the cysts are capable of surviving the acidic stomach
environment and eventually depositing in the ileum where they once again produce the
trophozoite. However, up to 90% of people infected with E. histolytica are asymptomatic or have
very mild disease . In children, cutaneous amebiasis almost always occurs in the anogenital or
perineal region as a result of direct inoculation from infected stool. This has been reported in
young children because of prolonged contact with fecal material in a child’s diaper. Ninety
percent of reported children with cutaneous amebiasis, including our patient, were associated
with diarrhea or dysentery. Alternatively, direct inoculation of the skin has also been reported
from scratching, anal or vaginal intercourse, and following surgical drainage or spontaneous
rupture of an abscess at a colostomy site or laparotomy incision . A higher incidence of infection
is reported among patients with low socioeconomic status and poor sanitation and hygiene .

The diagnosis of cutaneous amebiasis requires a high index of suspicion. The

characteristic cutaneous ulcer is well-demarcated, round, or oval, with heaped-up borders and an
erythematous halo. Ulcers are typically painful and bleed easily. The diagnosis can be made from
direct visualization of a fresh smear of the ulcer exudate or a scraping of the ulcer edge, which
will reveal motile trophozoites. Trophozoites or cysts can also often be demonstrated or cultured
from stool samples. Of note, cysts are often shed intermittently in the stool, so that multiple
specimens on different days may be required to demonstrate the parasite. Diagnostic serologic
tests, including indirect hemagglutination, enzyme-linked immunosorbent assay, latex
agglutination, and countercurrent immunoelectrophoresis, are both highly sensitive and specific
for amebiasis, but cannot reliably distinguish between past and current infection and often do not
become positive for a week or more after symptom onset .

Emetine has traditionally been the drug of choice for early diagnosed cutaneous
amebiasis. However, it can cause arrhythmia and thus requires hospitalization with cardiac
monitoring during administration. Dehydroemetine is a less toxic alternative that works well and
is often utilized in conjunction with diiodohydroxyquinolone or iodoquinol . Intestinal amebiasis
(which is usually seen in conjunction with cutaneous amebiasis in children) is treated with a two-
drug regimen. Metronidazole has become the drug of choice, followed by dehydroemetine,
chloroquine, or iodoquinol. No matter what the combination of drugs, the key to cure is early
diagnosis and prompt therapeutic intervention. Surgery may also be required in instances of
rapidly progressive and highly invasive disease.

Daftar pustaka

Alvarez-Chacon RA. Cutaneous amebiasis. Mod Probl Paediatr 2010;17:259–261.

Tanyuksel M, Petri WA. Laboratory diagnosis of amebiasis. Clin Microbiol Rev 2003;16:713–729.

Kenner, B. M., & Rosen, T. Cutaneous Amebiasis in a Child and Review of the Literature.
Pediatric Dermatology 2006;23(3), 231–234.